The overall goal of the Growth and Development Project is to investigate the effects of prenatal and postnatal exposures to polycyclic aromatic hydrocarbons [PAH], environmental tobacco smoke [ETS], and pesticides on child neurodevelopment from birth through the early school years. In this continuation of the cohort study, we propose to extend follow-up to 8 years of age, for the purpose of obtaining reliable measures of cognition, attention, and behavioral functioning with clear implications for subsequent adjustment and school performance. The cohort of mothers and children represent a high-risk minority population with widespread yet variable exposures to ambient and indoor toxicants and social adversities. Early results suggest that many of these children are experiencing potentially irreversible developmental impairment which may limit school readiness, behavioral competence, and ability to learn, even at relatively low levels of exposure. Based on findings of fetal growth deficits and impaired cognitive development at 2 years of age, we are concerned about longer-term trajectories and cascading effects, in which early deficits lead to later problems, often involving other functional domains. In this study, we expand the assessment of environmental risk to include multi-level exposures to chronic social stressors, in order to better understand how the social context buffers or exacerbates risk, rendering some children more vulnerable than others to the harmful effects of toxicants. Longitudinal follow-up permits us to identify early indicators (e.g., disruptive behaviors at 3 years) of later problems (attention deficit disorder with hyperactivity at 5 years), with implications for school performance and learning (teacher report at 7 and 8 years). A key feature of the study is the capacity to investigate the possible modulating role of genetic susceptibility (measured polymorphisms in metabolic activation and detoxification genes), nutritional factors (measured as plasma levels of antioxidant micronutrients), and chronic social stressors on the associations between environmental toxicants and neurodevelopment. We propose to: Aim 1. Quantify the impact of prenatal and postnatal exposures to air pollutants (PAH, ETS) and pesticides on neurobehavioral development through 8 years of age, after controlling for the effects of known determinants of child neurodevelopment and potential confounders. Aim 2. Refine the measurement of exposure to chronic social stressors to assess their impact on child neurobebavioral development at 5 and 7 years of age, and test interactions between environmental toxicants and stressors, by which some children are rendered more vulnerable than others to the toxic impact of pollutants. Aim 3. Investigate the modifying role of micronutrients and genetic polymorphisms on the association of toxic exposures (PAH and ETS) with fetal growth and neurodevelopment through age 7 years, as determined in Specific Aim 1. Aim 4. Collaborate with the Community Outreach, Translation and Application Core (COTAC) to translate research findings on neurodevelopmental risk associated with toxicant exposures, and assist in developing interventions and policies to prevent such exposures.